1,721,547 research outputs found
Noonan, D V, VX24209
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/407978Surname: NOONAN. Given Name(s) or Initials: D V. Military Service Number or Last Known Location: VX24209. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 43236.237030
Item: [2016.0049.40253] "Noonan, D V, VX24209
Noonan, D T, VX27000
No full textThis record was harvested from a previous catalogue system and will be withdrawn in 2025. Information in this record may be superseded or incomplete. Visit this record in UMA's new catalogue at: https://archives.library.unimelb.edu.au/nodes/view/407979Surname: NOONAN. Given Name(s) or Initials: D T. Military Service Number or Last Known Location: VX27000. Missing, Wounded and Prisoner of War Enquiry Card Index Number: 40608.237032
Item: [2016.0049.40254] "Noonan, D T, VX27000
Angiopoietin2 and tie2: tied to lymphangiogenesis and lung metastasis. New perspectives in antimetastatic antiangiogenic therapy
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Do Not Bite More Than You Can Chew: The Side Effects of Crowdfunding on Entrepreneurial Performances
No full textDecidual-like NK cell polarization: From cancer killing to cancer nurturing
Full text linkNatural killer (NK) cells accumulate at the fetal–maternal interface and represent 70% of immune cells in the decidua (dNK) at first-trimester pregnancy; they are immune-tolerant toward the semiallogenic fetus and are “nurturing” and nonkilling NK cells. A subset of NK cells in patients with cancer have features in common with dNK, which include expressing CD56, CD9, CD49a, and CXCR3, being poorly cytotoxic and proangiogenic, and mimicking the decidual nurturing role. In the oncologic patient, several factors can “decidualize” NK cells, turning them into immune-suppressant, growth-promoting proangiogenic cells. Here, we suggest ways to sharpen their blunted blades and intercept and curb their cancer-nurturing attitudes to restore their cytotoxic capabilities
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
The SARS‐CoV‐2 receptor, ACE‐2, is expressed on many different cell types: implications for ACE‐inhibitor‐ and angiotensin II receptor blocker‐based cardiovascular therapies
Full text linkSARS-CoV-2 is characterized by a spike protein allowing viral binding to the angiotensin-converting enzyme (ACE)-2,
which acts as a viral receptor and is expressed on the surface of several pulmonary and extra-pulmonary cell types, including
cardiac, renal, intestinal and endothelial cells. There is evidence that also endothelial cells are infected by SARS-COV-2,
with subsequent occurrence of systemic vasculitis, thromboembolism and disseminated intravascular coagulation. Those
effects, together with the “cytokine storm” are involved in a worse prognosis. In clinical practice, angiotensin-converting
enzyme inhibitors (ACE-Is) and angiotensin II receptor blockers (ARBs) are extensively used for the treatment of hypertension
and other cardiovascular diseases. In in vivo studies, ACE-Is and ARBs seem to paradoxically increase ACE-2 expression,
which could favour SARS-CoV-2 infection of host’s cells and tissues. By contrast, in patients treated with ACE-Is
and ARBs, ACE-2 shows a downregulation at the mRNA and protein levels in kidney and cardiac tissues. Yet, it has been
claimed that both ARBs and ACE-Is could result potentially useful in the clinical course of SARS-CoV-2-infected patients.
As detected in China and as the Italian epidemiological situation confirms, the most prevalent comorbidities in deceased
patients with COVID-19 are hypertension, diabetes and cardiovascular diseases. Older COVID-19-affected patients with
cardiovascular comorbidities exhibit a more severe clinical course and a worse prognosis, with many of them being also
treated with ARBs or ACE-Is. Another confounding factor is cigarette smoking, which has been reported to increase ACE-2
expression in both experimental models and humans. Sex also plays a role, with chromosome X harbouring the gene coding
for ACE-2, which is one of the possible explanations of why mortality in female patients is lower. Viral entry also depends
on TMPRSS2 protease activity, an androgen dependent enzyme. Despite the relevance of experimental animal studies, to
comprehensively address the question of the potential hazards or benefits of ACE-Is and ARBs on the clinical course of
COVID-19-affected patients treated by these anti-hypertensive drugs, we will need randomized human studies. We claim
the need of adequately powered, prospective studies aimed at answering the following questions of paramount importance
for cardiovascular, internal and emergency medicine: Do ACE-Is and ARBs exert similar or different effects on infection
or disease course? Are such effects dangerous, neutral or even useful in older, COVID-19-affected patients? Do they act on
multiple cell types? Since ACE-Is and ARBs have different molecular targets, the clinical course of SARS-CoV-2 infection
could be also different in patients treated by one or the other of these two drug classes. At present, insufficient detailed data
from trials have been made available
Marine algal antioxidants as potential vectors for controlling viral diseases
No full textAs the COVID-19 epidemic expands in the world, and with the previous SARS epidemic, avian flu, Ebola and AIDS serving as a warning, biomedical and biotechnological research has the task to find solutions to counteract viral entry and pathogenesis. A novel approach can come from marine chemodiversity, recognized as a relevant source for developing a future natural “antiviral pharmacy”. Activities of antioxidants against viruses can be exploited to cope with human viral infection, from single individual infections to protection of populations. There is a potentially rich and fruitful reservoir of such compounds thanks to the plethora of bioactive molecules and families present in marine microorganisms. The aim of this communication is to present the state-of-play of what is known on the antiviral activities recognized in (micro)algae, highlighting the different molecules from various algae and their mechanisms of actions, when known. Given the ability of various algal molecules—mainly sulfated polysaccharides—to inhibit viral infection at Stage I (adsorption and invasion of cells), we envisage a need to further investigate the antiviral ability of algae, and their mechanisms of action. Given the advantages of microalgal production compared to other organisms, the opportunity might become reality in a short period of time
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